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Vl Organic Solutes INTRODUCTION Selection of Agents . In selecting agents to be included in the organic contaminants section of this report, a number of tabulations of organic contaminants detected in drinking water were examined. From these lists, agents were selected that have been reported to be present in one or more drinking-water supplies at relatively high concentrations and for which there were data to suggest toxicity in man or animals. Also included were several agents that exhibit a structural relationship to other compounds for which toxicity data were available and all of the agents listed in the current interim standards, as well as those specific compounds listed in the Federal Register of December 24, 1975. A total of 298 volatile organic compounds were considered and 74 of these were selected for evaluation. Similar criteria were used to select the organic pesticides for inclusion In this report. Several additional agents were added after examination of the usage patterns for all major types of organic pesticides, as well as a number of agents that were considered to be potential contaminants of drinking-water supplies because of the large quantities produced. A total of 55 organic pesticides were selected for evaluation. 489

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490 DRINKING WATER AND H"LTH Evaluation of Toxicity A critical review of the available literature on the toxicology of each agent (or group of related agents) was carried out as the first stage in the evaluation. Although the primary focus in these reviews was on carcinogenesis and other chronic toxic effects, test results and data on teratogenesis, mutagenesis, reproductive ejects, metabolism, acute toxicity, and other types of studies were included when available. Information on the current production, manufacturing methods, and environmental distribution was included for some pesticides and other organic compounds. In the second stage of the evaluation, both the quantity and quality of the information in each of the critical reviews was considered to determine whether the data would permit judgments to be made regarding carcinogenicity or estimation of a maximum no-observed- adverse-e~ect level. The hazards of ingesting compounds that were assessed as confinned or suspected carcinogens were evaluated in terms of dose-related risks, as described below and in Chapter II. It is recognized that extrapolation of high-dose animal bioassay data to low-dose human exposures is beset by limitations, and that it is difficult to reconcile the results of experiments on animals that may show different target-organ responses, and may metabolize carcinogens at different rates and by different pathways. Such risk assessment and extrapolation procedures are further compromised by the limited information that is available concerning the mechanisms by which these agents act (e.g., as initiators, promoters, modifiers) and the almost total lack of data regarding the potentially synergistic and antagonistic interactions of these agents with each other and with other environmental agents. Despite these and other uncertainties, the "risk estimate" approach has been adopted as the basis for analyzing the data on carcinogenicity rather than the "safety factor" approach. After a substance had been identified as a carcinogen, the risk to man was expressed as the probability that cancer would be produced by continued daily ingestion over a 70 yr lifetime of 1 liter of water containing a standard quantity (1 ,ug/liter) of the substance in question. Estimates expressed in this form may then be used to calculate risk due to the concentrations actually found in drinking-water and the daily consumption. To make such estimates from the results of animal feeding studies, two steps are necessary. The first involves conversion of the standard human dose to the physiologically equivalent dose in the animal. This was performed on the basis of relative surface area (details are given in Hoel

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Organic Solutes 491 et al., 1975, Chapter II). The second step requires use of a risk model relating dose to eject. The model used for this purpose is p (~) = I - c,-(A,, + A, ~ + At d' + . . . A'. d') where P(a) is the lifetime probability that dose d (total daily intake) will produce cancer, K = the number of events in the carcinogenic process, and Ao,\~,A2, etc. . . . are nonnegative parameters (see Chapter II). At low doses, the higher-order terms in d2,a~, etc., may be neglected and P (d) ~ I _ {,-(A,, + APO ~ A`, + A, d No representing the background rate. When two or more sets of results of lifetime animal feeding studies were available, experimental values of P(a), the fraction of test animals developing cancer, and d, the total daily dose, were fitted to the equation to determine how many of the terms Ao,A~d,A2d2, etc., were necessary to give the best fit. Corresponding values Of Ao,A,, or X0, Al and \2, etc., were used to calculate Pep for the low-dose of interest, namely the animal dose that was physiologically equivalent to the standard dose for man. If the animal experiments involved only one dose level, the Aid term, alone, was used in the calculation. Upper confidence limits in the estimated low-dose risk were also calculated by use of maximum likelihood theory (Guess and Crump, 1976, Chapter II), and these values were tabulated. Since the animal data were obtained from lifetime feeding studies, the risk estimates calculated from them for the low-doses that were estimated to be physiologically equivalent to the human dose were taken to represent the lifetime risks for man. The background rate, obtained from the cancer incidence in the control groups of experimental animis and represented by the parameter ho, was excluded from the tabulated values of P(a), which therefore represent the incremental risks due to ingestion of the compounds in water. It was felt that predictions that are risk-related provide a more meaningful first approximation of hazard than safety-related predictions. The risk estimate approach may provide unique advantages for other areas of toxicological evaluations, such as mutagenesis, and it is recommended that the usefulness of this procedure be evaluated as a new predictive method in toxicology. For agents that were not considered to be known or suspected carcinogens and for which there were adequate toxicity data from prolonged ingestion studies in man or animals, the more traditional approach was utilized of combining the maximum dose producing no- observed-adverse-e~ects with an uncertainty (risk) factor to calculate an

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492 DRINKING WATER AND H"LTH ADI (acceptable daily intake). Several alternative terms, other than ADI, were considered, but it was concluded that the introduction of new terms might well lead to confusion and that the use of a widely recognized and generally acceptable term would be preferable for this report. The ADI has been used previously as an internationally established standard for the toxicologic evaluation of food additives and contaminants and the concept is applicable to other ingestion exposure situations. The ADI represents an empirically derived value that reflects a particular combina- tion of knowledge and uncertainty concerning the relative risk of a chemical. The uncertainty factors used to calculate ADI values in this report represent the level of confidence that was judged to be justified on the basis of the animal and human toxicity data. All calculations for an ADI were based on chronic feeding studies, but other considerations, e.g., mutagenicity, teratogenicity, and lack of sex and strain information, influenced the choice of the uncertainty factor. ADI values were not calculated for agents where the data were considered to be inadequate. Since the calculation of the ADI values is based on the total amount of a chemical that is ingested, the ADI values calculated in this report do not represent a safe level for drinking water. However, a suggested no- anticipated-adverse-e~ect level has been calculated for these chemicals in drinking water using two hypothetical exposures (where water constitutes 1% and 20~o of the total intake of the agent), and similar calculations can readily be made for other exposures. Conclusions The organic contaminants that have been identified in drinking water constitute a small percentage of the total organic matter present in water. Although approximately 9OYo of the volatile organic compounds in drinking water have been identified and quantified, these represent no more than logo of the total organic material. Of the nonvolatile organic compounds comprising the remaining 90~o of the total organic matter in water, only 5 to logo have been identified. From the 74 nonpesticide organic compounds and 55 organic pesticides selected for study, 22 have been identified as known or suspected carcinogens, 46 as having sufficient toxicity data to permit the calculation of an ADI value or a suggested no- adverse-effect level for drinking water, 6 as mutagens and 7 as teratogens. There were 61 agents for which the toxicity data were judged to be inadequate for establishing any recommendations. (See Tables VI-63 and 64 in "Summary of Organic Solutes.") It is evident that this effort constitutes only the beginning of a very large task. However, in preparing these reports and recommendations, an ~_

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Organic Solutes 493 attempt has been made to use procedures that will enable efforts in the future to be focused on revisions and additions to the estimates, adding to and updating, rather than on redoing, the task. Also identified are certain priorities for the selection of agents to be studied and the research needs in toxicology and epidemiology to facilitate the evaluation of the potential health hazards associated with organic agents that are or may be present in our drinking-water supplies. PESTICIDES: HERBICIDES Chloropheno~s 2,4D Introduction 2,4-D, or 2,4dichlorophenoxyacetic acid, was introduced as a plant growth-regulator in 1942 (USEPA, 1974b). It is registered in the United States as an herbicide for control of broadleaf plants and as a plant growth-regulator. Domestic use of 2,4-D is estimated at 40-50 million pounds a year, approximately 84% of which is used agriculturally and about 16% nonagriculturally (mainly for forest brush control). 2,4-D is produced commercially by chlorination of phenol to form 2,4 dichlorophenol, which reacts with monochloroacetic acid to form 2,4D (USEPA, 1974b). Commercial 2,4-D formulations are generally com- posed of the salts or esters (ethyl, isopropyl, buty1, amyl, hepty1, octyl, etc.) of the acid. Analysis of 28 samples of technical 2,4-D by gas chromatography showed that hexachlorodioxins were present in only one sample, at less than 10 ppm (Woolson et al., 1972~. The dioxin most likely to be formed, 2,7-dichlorodibenzo-p-dioxin, was not found. The major impurity in technical 2,4-D was identified as bis-~2,4dichIorophenox- y~methane, at 30 ppm (Huston, 1972~. The solubility of 2,4-D in water is 540 ppm at 20C; its major breakdown product, 2,4-dichlorophenol, is soluble at 4,500 ppm (USEPA, 1974b). The 2,4D salts are in general highly soluble, but the esters are much less soluble. 2,4D is chemically quite stable, but its esters are rapidly hydrolyzed to the free acid. Microbial degradation of 2,4-D contributes to its rapid breakdown (half-time, 1 week) in water (USEPA, 1974b). When exposed to sunlight or ultraviolet irradiation, aqueous 2,4D solutions decompose to 2,4-dichlorophenol, 4chlorocatechol, 2-hydroxy-4chlorophenoxy

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494 DRINKING WATER AND H"LTH acetic acid, 1,2,4benzene trial, and polymeric humic acids. The overall breakdown rate of 2,4D in aqueous solution is fairly high, and 2,4- dichlorophenol is even more photolabile. Most 2,4-D residues are retained in the soil, where breakdown usually occurs within 6 weeks. Between 1964 and 1970, only 50 samples of food were found to be contaminated with 2,4-D; the concentrations detected were 0.021~.16 ppm (USEPA, 1974b). Residues were found in 1% or less of dairy products, oils, fats and shortening, and fruit, in 1.9% of leafy vegetables, and in 22.1% of sugar and adjuncts. 2,4D is found in water (Marigold and Schulze, 1969~. Concentrations as high as 70 ppb have been detected in Oregon streams after aerial application to forestland (Hiatt, 1976~. 2,4-D was detected in raw water at 0.05 ,ug/liter, in Lafayette, Indiana (USEPA, 1975j). The EPA has set an interim standard for 2,4-D in finished water of 0.1 mg/liter (USEPA, 1975i). Metabolism When 2,4-D with labeled carbon was administered orally to sheep, 96% of the dose was excreted unchanged in the urine in 72 h, slightly less than 1.4% in the feces (Clark et al., 1964~. When adult sheep and cattle were fed 2,4-D in the diet for 28 days at up to 2,000 ppm, the kidney contained the highest and the liver somewhat lower concentrations of 2,4-D and its breakdown product 2,4-dichlorophenol (Clark et al., 1975~. Withdrawal from treatment for 7 days resulted in almost complete elimination of 2,4- D and its major metabolite from the tissues. In rats that received 1-10 mg of 2,4D, there was almost complete excretion in the urine and feces in 48 h; at higher doses, some accumulation occurred in tissues (Khanna and Fang, 1966~. After subcutaneous injection of 2,4-D and its butyl and isoocty} esters into mice at 100 mg/kg, the esters were eliminated rapidly, and only 5- 10% of the 2,4-D remained after 1 day (USEPA, 1974b). No 2,4 dichlorophenol was detected in extracts of the treated mice. In feeding studies of 2,4-D with dairy cows and steers, unchanged 2,4- D was found only in the urine (Bache et al., 1964a, b; Guteman et al., 1963a, b; Lisk et al., 1963~. Other studies (Burchfield and Storrs, 1961; Klingman et al., 1966) demonstrated that 2,4D was eliminated in the milk of cows maintained in pastures treated with 2,4-D or its butyl or isooctyl ester. The pharmacokinetic profile of 2,4D has been determined in five male human volunteers (Sauerhoff et al., 1976~. After ingestion of a single 5- mg/kg oral dose, 2,4-D was eliminated from plasma in an apparent first

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Organic Solutes 495 order process with an average half-life of 11.7 h. All subjects excreted 2,l D in the urine with an average half-life of 17.7 h, mainly as free 2,4-D (82.3~o), with a smaller amount excreted as a 2,~D conjugate (12.8~o). Health Aspects Observations in Man A 46-yr-old male farmer accidentally ingested a 2,4-D formulation; the dose was estimated to contain 2,4-D at 100 mg/kg, S-ethyldipropylthiocarbamate at 230 mg/kg, and epichlorohy- drin at 2.3 mg/kg (Berwick, 1970~. The clinical picture was indicative of 2,4-D poisoning with symptoms including fibrillate twitching and muscular paralysis. Serum glutamic oxalacetic transaminase, glutamic pyruvic transaminase, lactic dehydrogenase, aldolase, and creatine phosphate were increased, and both hemoglobinuria and myoglobinuria were observed. After recovery of the patient, there was also a 4-month loss of sexual potency. In testing 2,4-D for possible use in disseminated coccidiomycosis, 18 intravenous doses were administered to a patient over a 33-day period, with no observed side effect (Seabury, 1963~. The dosage was 15 mg/kg for the last 12 doses, except that the eighteenth was increased to 37 mg/kg. Following the nineteenth and final dose of 67 mg/kg, the patient exhibited fibrillary twitching and general hyporeflexia. The patient later died, apparently owing to the disease. After a 23-yr-old man used 2,4-D in suicide, the lethal dose was estimated to be over 90 mg/kg (Nielsen et al., 1965~. Assouly (1951) is reported to have taken 2,4-D daily at 8 mg/kg for 3 weeks without harmful erects. Data from Dow Chemical Co. (Johnson, 1971) on 220 workers exposed to 2,4-D at 0.43-0.57 mg/kg/day over a period of 0.5-22 yr showed no significant differences from data on an unexposed human population. Observations in Other Species Acute Elects The acute toxicity of 2,4-D is moderate in a number of animal species, with LD50 values of 10~541 mg/kg for rats, mice, guinea pigs, chicks, and dogs (Drill and Hiratzka, 1953; Rowe and Hymas, 1954~. Salts and esters of 2,4-D show an even lower degree of acute toxicity. The acute oral toxicity of the major 2,4-D breakdown product 2,4- dichlorophenol is 580 and 1,625 mg/kg for the rat and the mouse, respectively (Toxic Substances List, 1974~.

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496 DRINKING WATER AND H"LTH Subchronic and Chronic Effects Young adult female rats were given oral doses of 2,4-D in olive oil at 0, 3, 10, 30, 100, and 300 mg/kg five times a week for 4 weeks (Rowe and Hymas, 1954~. No adverse effects were noted at 30 mg/kg and below, but depressed growth rates, liver pathology, and gastrointestinal irritation occurred at 300 mg/kg. In another experiment (Rowe and Hymas, 1954), depressed growth, liver pathology, mortalities, and increased liver/body weight ratios were observed in rats fed 1,000 ppm 2,4-D for 113 days. 2,4-D was administered orally to dogs at dosage levels of 0, 2, 5, 10, and 20 mg/kg 5 days a week for 13 weeks (Drill and Hiratzka, 1953~. Three of four animals receiving 20 mg/kg dose died within 49 days. These animals showed a definite decrease in the percentage of lympocytes in the peripheral blood. The surviving animals in all groups did not show any hematological abnormalities. Dietary levels of 0, 5, 25, 125, 625, and 1,250 ppm technical grade 2,4-D were fed to female and male Osborne-Mendel rats for 2 yr (Hansen et al., 1971~. No significant ejects were observed on growth, survival rate, organ weights, or hematologic parameters. There was also no elevated incidence of tumors over that seen in controls. In a parallel study (Hansen et al., 1971), groups of 6-8-month-old beagle dogs received 0, 10, 50, 100 and 500 ppm of technical 2,4-D for 2 years. No 2,4-D related ejects were noted. None of the lesions observed in the 30 dogs were believed related to the treatment. The no-adverse-effect level of 2,4-D in the dog has been established at 8 mg/kg/day (Lehman, 1965~. Mutagenicity 2,4-D was unable to induce point mutations in four microbial systems (Andersen et al., 1971) and showed no activity in Drosophila (Vogel and Chandler, 1974~. Saccharomyces cerevisiae strain D4 (5 x 106) was treated with 2 ml of an aqueous 2,4-D suspension (trade name, U46D-Fluid) (Siebert and Lemperle, 1974~. The mitotic gene conversion frequency of the ade 2 locus was increased fivefold above control values; that of the try 5 locus was increased sixfold above control values. Carcinogenicity Studies on the in vitro and in viva eject of 2,~D on the growth of Ehrlich ascites tumor in BALB/c mice showed that the herbicide was inhibitory at 45 mg/kg or more (Walker et al., 1972~. There was no significant increase in the incidence of tumors in various mouse strains initially given 2,4-D or its esters at 46.4 mg/kg/day orally on days 7-28 followed by dietary feeding up to 323 ppm for 18 months (USEPA, 1974b). In another study, mice that received 2,4-D orally for their life

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Organic Solutes 497 span showed no increased incidence of tumor formation (Vettorazzi, 1975b). A study (Arkhipor and Kozlova, 1974) reported that two rats developed fibroadenoma and one hemangioma 27-31 months after receiving one-tenth the LD50 of the amine salt of 2,4-D. Administration of 0.1 the LD50 dose of the amine salt orally or subcutaneously to mice produced no tumors after 33 months. The herbicide, however, had a cocarcinogenic erect in mice when it was applied to the skin with 3- methylcholanthrene. DNA synthesis was increased, and there was a loss of cell differentiation in cultured chicken muscle after treatment with high concentrations of 2,4-D (Haag et al., 1975~. 2~4-Dichlorophenol has not been tested for carcinogenicity alone (USEPA, 1974b), but it is an initiator for skin carcinogenesis (Boutwell and Bosch, 1959~. Reproduction In a three-generation, six-litter Osborne-Mendel rat reproduction study, no deleterious erects due to technical 2,4-D at dietary doses of 100 or 500 ppm were observed (Hansen et al., 1971~. At 1,500 ppm, however, 2,4-D, although affecting neither fertility of either sex nor litter size, sharply reduced the percentage of pups that survived to weaning and the weights of the weanlings. Teratogenicity In studies of CD-1 mice, Courtney (cited in EPA, 1974b) found that 2,4-D at 221 mg/kg per day increased fetal mortality, but produced no cleft palates. Various 2,4-D esters (isopropyl ester at 147 mg/kg/day, n-butyl ester at 155 mg/kg/day, and isooctyl ester at 186 mg/kg/day) had no erect on the incidence of cleft palate or fetal mortality, but did affect fetal weight. A significant increase in cleft palate was found, however, after administration of the propylene glycol butyl ether ester at 195 mg/kg/day. A statistically significant increase in the proportion of abnormal fetuses was reported in mice that received maximally tolerated subcutaneous doses of the isooctyl ester, and two isopropyl esters of 2,4-D (130, 100, and 94 ,ug/kg, respectively), in dimethyl sulfoxide (DMSO) solution (Mrak, 1969~. DMSO itself, however, is a teratogen (Caujolle et al., 1967~. Bage et al. (1973) observed teratogenic and embryotoxic erects in NMRI mice that received 50- or 110-mg/kg injections of 2,4-D on days ~14 of gestation. Pregnant rats were treated orally with 2,4-D at 12.5, 25, 50, 75, and 87.5 mg/kg/day (maximal tolerated dose) or equimolar doses of propylene glycol butyl ether ester of 2,4-D up to 142 mg/kg/day or isooctyl ester of 2,4-D up to 131 mg/kg/day on days ~15 of gestation (Schwetz et al.,

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498 c L. _ 3 C) US ~ Ct i_ -4 LO 2 C. O ~ a.) ~ 'C: ~ ~ > cez ~ 3 V, ._ In ~ _ <( _~ 0 3= O ma ~ Ct PA o 4 - ._ ._ o m O ~ _ 3 Ct ~q o3 `,_ ._ C) C~ ~0N V ~_ ', y^~\ _ ~ ~1 C ~- (~) ~C) x 2 x o o o _ ~ _ C C ~ ~o y E E C ~ E - o.8= ~oo ~ V~ - Ct - _ Cd 0,, - C) ~.O X ~_ ._ o - o ~ _ ~ o o C: C Ct - o ~ r~ - - u) cd - ~ . o - .o~ xct -- o~ d c) v~ - ~L CL ~ (t - ~rC . - o ^ `,, 8^ ~_ os ~ 0 0 0 ~Y ~1 ~o ~ 3 ,, 3 ;^ ~c _ r ~'d 3 Ct ~0 os as os _ _ C O O O Ct ~oo ~ C o o C,, 11 ._ ~ ~_ ~o Ct 3 x ._ Ye ._ ._ - - :7 E E E 4 E E ~ ~ e -~ ~6 ~ v) 00- bO-~ OD O o O O O t30 o X - o o - 6 - - Y 0c - o o 11 O . o _ _ V) r~ o 11 os o o C ~d ~o r~ o 3 0 C _ O ~ ~_ ~n O ._ ~o C. _ 4 - C ._ ~ o 11 - O~ _O C(_ ~ = C~ ~ .O r~ ~ eD C`' ~ ed t c (~, ~ ~ 3 C ~ (LI) ~ _ a~ ,^ 1 ~o o ~ ~ 11 ~ ~ Ool) _ t,_ ~ ~ o C 3 c ~c C ~o ~ oo o ~ ~o _ C 3 11 ^-C ~ ~ O ~ ~ 3 ~ c~ c~ ~o 3 ~ C ~ C V) ~ _ ~ ~ ~ Ct U) ~ ~ ;> ~

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Organic Solutes 499 1971~. Fetotoxic responses were seen at the high dosages, but teratogenic ejects were not seen at any dosage. The authors suggested that the no- adverse effect dosage of 2,4-D (or the molar equivalent, in the case of the esters) was 25 mg/kg/day. Prenatal studies on 2,4-D in Wistar rats showed that it induced fetotoxic ejects and an increased incidence of skeletal anomalies after single oral doses of 100 150 mg/kg/day on days 6 15 of gestation (Khera and McKinley, 1972~. At the highest dosage of 150 mg/kg/day, the isooctyl ester, and butyl ester, and butoxyethynol and dimethylamine salts of 2,4-D were all associated with significantly increased teratologic incidence. The butyl and isooctyl esters also tended to decrease fetal weight. At a lower dosage, 2,4-D and its salts and esters induced no apparent harmful effects. Pregnant hamsters received technical 2,4-D (three samples) at 20, 40, 60, and 100 mg/kg/day orally on days 6 10 of gestation (Collins and Williams, 1971~. Terata were produced occasionally with 2,4-D, and the fetal viability per litter decreased; but neither eject was clearly dose- related. The lowest dose causing fetal anomalies with the three technical 2,4-D samples was 60 mg/kg/day. Conclusions and Recommendations The acute toxicity of 2,4-D is moderate. No-adverse-effect doses for 2,4- D were up to 62.5 mg/kg/day and 10 mg/kg/day in rats and dogs, respectively. Based on these data, an ADI was calculated at 0.0125 mg/kg/day. The available data on subchronic and chronic toxicity and calculations of ADI are summarized in Table VI- 1. The acceptable daily intake of 2,4-D has been established at 0.3 mg/kg by FAD/WHO. On the basis of electron-capture gas chromatography, the detection limit for 2,4-D in water is 1 ppb. There are substantial disagreements in the results of subchronic and chronic toxicity studies with 2,4-D, perhaps reflecting the use of different formulations or preparations. In view of these deficiencies and the variability of the results, additional, properly constituted toxicity studies should be undertaken. 2,4,5-T AND TCDD Introduction 2,4,5-T, or 2,4,5-trichlorophenoxyacetic acid, was introduced in 1944 as a translocated, selective herbicide; it is applied after emergence and is

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